Influence of a 50 Hz magnetic field and of all-trans-retinol on the proliferation of human cancer cell lines

Riferimento: 
Int J Oncol. 2012 May;40(5):1405-13.
Autori: 
Trillo MA, Martínez MA, Cid MA, Leal J, Úbeda A. angeles.trillo@hrc.es
Fonte: 
Int J Oncol. 2012 May;40(5):1405-13.
Anno: 
2012
Azione: 
La risposta di due linee di cellule umane di neuroblastoma (NB69) ed epatocarcinoma (HepG2) a trattamento intermittente con un debole (100 microtesla) campo magnetico a 50 Hz di frequenza (MF), da solo o in combinazione con 0.5 microM all-trans retinolo (ROL), mostra che entrambi gli agenti, un MF debole e ROL a bassa concentrazione, inducono risposte proliferative nelle due linee cellulari umane saggiate.
Target: 
MF-ROL/neuroblastoma, epatocarcinoma.

ABSTRACT
In vitro exposure to power frequency magnetic fields (MF) has been reported to influence cell proliferation and differentiation. However, the nature of the response of different human cancer cell types to these fields has not been sufficiently characterized. The present work investigates the response of two proliferating human cell lines of neuroblastoma (NB69) and hepatocarcinoma (HepG2) to a 42 h, intermittent treatment with a weak, 100 µT, 50 Hz MF, alone or in combination with 0.5 µM all-trans-retinol (ROL), a retinoid currently applied in oncostatic therapies. In each experimental replicate the cell samples were submitted to one of the following treatment combinations: MF+/ROL+, MF+/ROL-, MF-/ROL+ or MF-/ROL-. The proliferative response was determined by cell counting (Trypan blue exclusion), BrdU incorporation and by spectrophotometric analysis of total protein and DNA content. The results show that when administered separately, the two treatments, MF and ROL, significantly enhanced cell proliferation in both cell lines. In NB69 simultaneous administration of MF and ROL induced an additive effect on cell proliferation, associated to increased DNA content. By contrast, in HepG2 the ROL-induced cell proliferation and increased protein content were partially blocked by simultaneous exposure to MF. Taken together, these data show that both agents, a weak MF and ROL at a low concentration, induce proliferative responses in the two assayed human cell lines. However, significant differences were observed between the responses of the two cellular species to the combined treatment with ROL and MF, indicating that the mechanisms underlying the cellular response to each of the two agents can mutually interact in a manner that is cell type-specific.

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